Nutrition, Metabolism, and Body Temperature Regulation
Even during prolonged fasting or starvation, the body
sets priorities. Muscle proteins are the ﬁrst to go (to be cat-
abolized). Movement is not nearly as important as main-
taining wound healing and the immune response. But as
long as life continues, so does the body’s ability to produce
the ATP needed to drive life processes.
Of course there are limits to the amount of tissue protein
that can be catabolized before the body stops functioning.
±e heart is almost entirely muscle protein, and when it
is severely catabolized, the result is death. In general, the
amount of fat the body contains determines the time a per-
son can survive without food.
Even collectively, all of the manipulations aimed at increasing
blood glucose are not enough to supply energy for prolonged
fasting. Luckily, the body can adapt to burn more fats and pro-
teins, which enter the Krebs cycle along with glucose break-
down products. ±e increased use of noncarbohydrate fuel
molecules (especially triglycerides) to conserve glucose is called
As the body progresses from the absorptive to the postab-
sorptive state, the brain continues to take its share of blood glu-
cose, but virtually every other organ switches to fatty acids as its
major energy source, sparing glucose for the brain. During this
transition phase, lipolysis begins in adipose tissues. Tissue cells
pick up released fatty acids and oxidize them for energy. In ad-
dition, the liver oxidizes fats to ketone bodies and releases them
to the blood for use by tissue cells.
If fasting continues for longer than four or ﬁve days, the
brain too begins to use large quantities of ketone bodies as well
as glucose as its energy fuel. ±e brain’s ability to use an alterna-
tive fuel source has survival value—much less tissue protein has
to be ravaged to form glucose.
Hormonal and Neural Controls
of the Postabsorptive State
±e sympathetic nervous system interacts with several hor-
mones to control events of the postabsorptive state. Conse-
quently, regulation of this state is much more complex than
that of the absorptive state when a single hormone, insulin,
An important trigger for initiating postabsorptive events is
reduced insulin release, which occurs as blood glucose levels
drop. Falling insulin levels inhibit all insulin-induced cellular
responses. Interestingly, drinking moderate amounts of beer,
wine, or gin before or during a meal improves the body’s use of
insulin. ±at is, it lowers blood glucose without increasing in-
sulin release. ±e advantage of this is obvious because although
blood glucose naturally spikes a²er a meal, prolonged elevation
can increase the risk of diabetes mellitus and heart disease.
Declining glucose levels also stimulate the alpha cells of the
pancreatic islets to release the insulin antagonist
other hormones acting during the postabsorptive state, glu-
cagon is a
—it raises blood glucose
Blood glucose levels remain high, and large amounts of glucose
are excreted in urine. Metabolic acidosis, protein wasting, and
weight loss occur as large amounts of fats and tissue proteins
are used for energy. (Chapter 16 describes diabetes mellitus in
±e postabsorptive state, or
is the period when the
GI tract is empty and body reserves are broken down to supply
energy. Net synthesis of fat, glycogen, and proteins ends, and ca-
tabolism of these substances begins to occur
±e primary goal during the postabsorptive state is to maintain
blood glucose levels within the homeostatic range (70–110 mg
of glucose per 100 ml). Remember that constant blood glucose
is important because the brain almost always uses glucose as its
energy source. Most events of the postabsorptive state either make
glucose available to the blood or save glucose for the organs that
need it most by using fats for energy.
Sources of Blood Glucose
So where does blood glucose come from in the postabsorp-
tive state? Sources include stored glycogen in the liver and
skeletal muscles, tissue proteins, and, in limited amounts,
fats (Figure 24.20b).
Glycogenolysis in the liver.
±e liver’s glycogen stores (about
100 g) are the ﬁrst line of glucose reserves. ±ey are mobi-
lized quickly and eﬃciently and can maintain blood sugar
levels for about four hours during the postabsorptive state.
Glycogenolysis in skeletal muscle.
Glycogen stores in skel-
etal muscle are approximately equal to those of the liver.
Before liver glycogen is exhausted, glycogenolysis begins
in skeletal muscle (and to a lesser extent in other tissues).
However, the glucose produced is not released to the blood
because, unlike the liver, skeletal muscle lacks the enzymes
needed to dephosphorylate glucose. Instead, glucose is
partly oxidized to pyruvic acid (or, during anaerobic condi-
tions, lactic acid), which enters the blood, is reconverted to
glucose by the liver, and is released to the blood again. ±us,
skeletal muscle contributes to blood glucose homeostasis
indirectly, via liver mechanisms.
Lipolysis in adipose tissues and the liver.
Adipose and liver
cells produce glycerol by lipolysis, and the liver converts the
glycerol to glucose (gluconeogenesis) and releases it to the
blood. Because acetyl CoA, a product of the beta oxidation
of fatty acids, is produced beyond the
steps of gly-
colysis, fatty acids
be used to bolster blood glucose
Catabolism of cellular protein.
Tissue proteins become the
major source of blood glucose during prolonged fasting
when glycogen and fat stores are nearly exhausted. Cellu-
lar amino acids are deaminated and converted to glucose
in the liver. During fasts lasting several weeks, the kidneys
also carry out gluconeogenesis and contribute as much glu-
cose to the blood as the liver.